The discovery of vanadium as an essential nutrient in animals has furthered the need for understanding the biochemical role of this element. Symptoms of vanadium deficiency in laboratory animals include impairment of growth and reproductive performance, altered bone structure, hypercholesterolemia, and hyperlipidemia. Vanadium deficiency can be induced in rats by maintenance from day two in utero on a diet containing from 0.015 to 0.030 ppm vanadium. The influence of vanadium on cholesterol metabolism will be examined from the standpoint of its transport, synthesis, and excretion. Phospholipid metabolism in connection with lipid mobilization will be investigated with regard to hyperlipidemia. A search for tissue-specific binding sites will involve tissue vanadium analysis and V48-uptake in deficient and control rats. The mechanism of vanadium transport in serum will also be investigated following V48-administration. Vanadium may influence the metabolism of other trace minerals. Tissue levels of Fe, Zn, Cu, and Mn will be compared in control and deficient rats. Vanadium deficiency would most likely occur in humans as a mild or chronic form. Therefore, long term deficiency will be examined in the rat. The following parameters will be monitored at regular intervals throughout a 48 month period: plasma triglycerides and cholesterol, packed cell volume, plasma glucose, plasma vanadium, and reproductive performance. The relationship between dietary and plasma vanadium will be examined. Efforts will be made to correlate an easily-measured clinical parameter with vanadium deficiency in order to develop a model system for human studies.